Class, action Flashcards
H2 (histamine 2) antagonist
Secretion affecting, decreases acid and pepsin in response to gastrin by blocking H2 receptor sites
Antacids
Secretion affecting, neutralizes HCl
PPIs (proton pump inhibitors)
Secretion affecting, decrease HCl at lumen
GI protectant
Secretion affecting, protects ulcer sites by adhering to them in duodenum
Prostaglandin
Secretion affecting, inhibits acid, increases bicarbonate and mucous in stomach
Digestive enzymes
Secretion affecting, replacement therapy to breakdown foods
Chemical stimulants
Motility affecting, irritate nerve plexus to increase motility starting at small intestine
Bulk stimulants
Motility affecting, increase motility by increasing feces size this increasing fluid and stretch for stimulation
Osmotic laxatives
Motility affecting, increased water in GI causing increase in motility
Lubricants
Motility affecting, increased feces viscosity
(see other cards for the 3 specific lubricants)
Docusate
Lubricant, detergent action on intestinal bolus, leads to softer stool
Glycerin
Lubricant, gentle evacuation due to softer stool from hyperosmolar effects (water pulled in), no systemic affects
Mineral oil
Lubricant, forms slippery coat on contents of intestinal tract
GI stimulant
Motility affecting, stimulates parasympathetic leading to increased GI secretions and motility
Antidiarrheal
Motility affecting, decreased motility by directly acting on GI lining
Phenothiazines
Antiemetic, suppresses CNS by stimulating medulla to decrease nausea and vomiting,
Also is an anti anxiety drug
Nonphenothiazine
Antiemetic, decreases vomiting by decreasing responsiveness in the nerve cells that induce vomiting in the CTZ (chemoreceptor trigger zone)
5-HT3 (serotonin) receptor blockers
Antiemetic, blocks receptor sites associated with nausea and vomiting peripherally and in CTZ (chemoreceptor trigger zone)
Substance P/Neurokinin 1 receptor antagonists
Antiemetic, act directly in CNS to block receptors associated with nausea and vomiting
Dronabinol and nabilone
Antiemetic, contain active ingredient of cannabis
Hydroxyzine
Antiemetic, suppression of CNS cortical areas
Trimethobenzamide
Antiemetic, less sedation/CNS suppression
Immune stimulants
Interferons
Interleukins
Colony stimulating factors
Interferons
Immune stimulants, prevent virus replication, inhibit tumor growth, for cancer and warts
Interleukins
Immune stimulants, increase NK and lymphocytes to activate cellular immunity and decrease tumors
Colony stimulating factors
Immune stimulant, decrease infection in patients with bone marrow suppression, help treat blood related cancers
Immune suppressants
Immune modulators
T and B cell suppressors
Interleukin receptor antagonists
Monoclonal antibodies
Immune modulators
Immune suppressant, decrease pro inflammatory cytokines and increase anti inflammatory cytokines
T and B cell suppressors
Immune suppressant, decrease antibodies produced by B cells, decrease suppressor and helper T
Interleukin receptor antagonist
Immune suppressant, block interleukins to treat RA
Monoclonal antibodies
Immune suppressant, attach to specific receptors, disable T cells
Salicylates
Analgesic/antipyretic/anti inflammatory, decrease prostaglandin
NSAIDs
Analgesic/strong anti inflammatory/ also antipyretic, block COX-1 and COX-2 and decrease prostaglandin
Acetaminophen
Antipyretic/analgesic effects/ NOT anti inflammatory, decrease prostaglandin, act on thermoregulatory cells of hypothalamus
Gold compounds
Anti arthritis, absorbed by macrophages leading to decreased phagocytosis and decreased tissue destruction at joints
DMARDs (TNF Blockers)
Anti arthritis, used before joint damage, decreased local effects of TNF - which is a cytokine that kills tumors and stimulates inflammation
Glucocorticoids
Adrenal corticoid, enter cells to bind to cytoplasmic receptors to have anti inflammatory and immuno suppressant effects- for autoimmune disorders, COPD, RA
Mineralocorticoids
Adrenal corticoid, works like aldosterone, holds Na, water follow Na, water levels in body increase, K is excreted- replacement therapy for Addison
Antitussives
Upper respiratory, act on medulla to decrease cough reflex
Topical nasal decongestant
Upper respiratory, decreases edema and inflammation via local vasoconstriction
Oral decongestants
Upper respiratory, stimulates alpha Adrenergic in nasal membrane leading to membrane shrinkage, drainage, and improved airflow
Topical nasal steroid decongestant
Upper respiratory, decreased inflammation
Antihistamines
Upper respiratory, decreased histamine at H1 receptor, decreasing allergic response;
Anticholinergic and antipruritic effects;
more sedation with 1st gen
Expectorants
Upper respiratory, increased output of respiratory tract fluids by decreasing adhesiveness and surface tension leading to easier movement;
Less sticky = easier to cough up
Mucolytics
Upper respiratory, BREAKDOWN mucous to aid high risk respiration patient cough up thick and tenacious secretions
Xanthines
Bronchodilator AKA antiasthmatic/
Lower respiratory, direct effect on smooth muscle at respiratory tract in bronchi and blood vessels
Sympathomimetics
Bronchodilator AKA antiasthmatic/lower respiratory, beta 2 selective Adrenergic agonists, dilate bronchi, increased respiratory rate and depth
SABA
LABA
Anticholinergic
Bronchodilator AKA antiasthmatic/lower respiratory, decreased vagal effects leading to relaxed smooth muscle at bronchi
Inhaled steroids
Lower respiratory, decreased inflammation in airways
Leukotreine receptor antagonists
Lower respiratory, decreased leukotrine production
Lung surfactants
Lower respiratory, replaces missing surfactant in neonates with RDS
Nitrates
Angina, helps restore appropriate supply and demand ratio of oxygen delivery to the myocardium;
Acts directly on smooth muscle to cause relaxation and decreased muscle tone of blood vessels;
Causes vasodilation
Beta blockers
Angina, block SNS leading to decrease CO and renin release, decreased blood volume and HR; vasodilation
Calcium channel blockers
Prinzmetal angina, Inhibit Ca movement across cells of myocardial and arterial muscles; alters action potential and blocks muscle cell contraction
Cardiac glycosides
For HF, increase squeeze and CO and renal perfusion and output, lowers blood volume and HR and conduction velocity through AV node;
Positive inotrope/negative chronotrope;
Increases intracellular Ca, diuretic effect and decreased renin release
Phosphodiesterase inhibitors
For HF, block Phosphodiesterase which leads to increased cAMP and intracellular Ca, stronger squeeze and prolonged response to SNS stimulation; directly relaxes ventricular smooth muscle
HCN channel blockers
For HF, slows SA node in repolar phase to decrease work by heart
Class 1
Antiarrhythmics, decreases depolarization and automaticity of ventricular cells to increase ventricular fibrillation threshold;
“Sodium channel blocker”
Class 2
Antiarrhythmics, block beta to depress phase 4 of action potential to decrease HR and cardiac excitability and CO; slows conduction through AV
Class 3
Antiarrhythmics, blocks K to slow outward flow of K during phase 3 to prolong phase 3
Class 4
Antiarrhythmics, block Ca movement across membrane to decrease action potential and delay phase 1 and 2 of repolarization; this slows automaticity and conduction through AV node and slows HR
Adenosine
Antiarrhythmics, converts SVT to sinus rhythm; stops heart temporarily
Digoxin
As an antiarrhythmic, it slows Ca from leaving cell which prolongs action potential and conduction and HR
Dronedarone
Antiarrhythmics, decreases risk of hospitalization in patients with AF or flutter with CVD risk factors and are in sinus rhythm
ACE
RAAS BP drug, Inhibits angiotensin 1 to 2 enzyme, blocking aldosterone which leads to vasodilation and excretion of Na and water
ARBs
RAAS BP drug, angiotensin 2 receptor antagonist, prevents vasoconstriction and aldosterone release
Renin inhibitors
RAAS BP drugs, inhibits renin thus inhibiting RAAS, lowering BP and aldosterone and Na reabsorption
Vasodilators
BP drug, directly act on smooth muscle to relax and lower BP with dilation and increasing CO
Alpha Adrenergic blockers (non selective)
SNS blocking BP drugs, blocks alpha 1 leading to vasodilation and lower BP;
Alpha 2 blocker prevents NE feedback loop
Alpha 1 blockers
SNS blocking BP drugs, decreases vascular tone leading to vasodilation and lower BP
Alpha and beta (non selective)
SNS blocking BP drugs, blocks NE at all alpha and beta receptors in the SNS leading to decreased BP and HR and increased renal perfusion and decreased renin
Alpha 2 agonist
SNS blocking BP drugs, stimulates alpha receptors in CNS and inhibits CV centers which leads to decreased sympathetic outflow from CNS thus lower BP
Antihypotensive drugs (vasopressors)
BP drugs, stimulate all Adrenergic receptors in SNS leading to increased HR and contractility and increased BP and constriction and bronchodilation thus increased respiratory rates and depth
Antiplatelet agents
Coagulation drug, block receptor site at platelet membrane to alter formation of plug
Anticoagulant agents
Coagulant drugs, interfere with clotting cascade
Thrombolytic agents (clot busters)
Coagulant drugs, activate plasminogen to plasmin leading to fibrin breaks thus dissolved clot
Vitamin K
Anticoagulant adjunct, warfarin antidote
Lepirudin
Anticoagulant adjunct, HIT (heparin allergic reaction) treatment
Protamine sulfate
Anticoagulant adjunct, heparin antidote
Antihemophilic
Coagulant drug, replaces missing factors to prevent blood loss from injury or surgery and treat bleeding disorders
Hemostatic agents
Coagulant drug, systemic: prevent systemic clot breakdown to prevent blood loss; topical: for surface injuries involving so much damage to small vessels in area that clotting doesn’t occur and blood is slowly and continuously lost (road rash)
